The effects of fasting and refeeding on the glucose transport response to insulin in isolated rat adipose cells have been examined. The results suggest that the insulin resistant glucose transport in isolated adipose cells from fasted rats can be explained by a decreased translocation of glucose transporters to the plasma membrane due to a depleted intracellular pool. In contrast, the insulin hyperresponsive glucose transport observed with refeeding appears to result from 1) a restored translocation of glucose transporters to the plasma membrane from an intracellular pool repleted through an increase in intracellular protein and 2) enhanced plasma membrane glucose transporter intrinsic activity. The human Hep G2 glucose transporter cDNA clone has been used to examine the molecular basis for these alterations. The data suggest that the abundance of mRNAs for multiple adipose cell genes is affected by fasting and refeeding. In particular, this is the first demonstration in an insulin-sensitive tissue that glucose transporter number, and hence a major factor in the glucose transport response to insulin, may be controlled, at least in part, by alterations in mRNA abundance. Insulin increases glucose transport activity and IGF-II binding in rat adipose cells by eliciting the redistribution of glucose transporters and IGF-II receptors from large intracellular pools to the plasma membrane. We now have measured cell surface IGF-II binding in intact cells from 2-day fasted and 2-day fasted/6-day refed rats and assessed IGF-II receptor number in subcellular membrane fractions by immunoblotting. The results suggest that fasting differentially regulates the number and distribution of IGF-II receptors and glucose transporters in adipose cells. This finding suggests distinct intracellular trafficking pathways for these proteins. Nutritional regulation of the IGF-II receptor may serve as a tool to explore the physiological role of IGF-II.